Vertigo — Causes, BPPV, Epley Manoeuvre & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Vertigo is the illusion of self-motion or environmental motion — typically experienced as a spinning, tilting, rocking, or tumbling sensation — in the absence of actual movement. It is caused by asymmetric signals from the vestibular system (the balance organs in the inner ear and their central connections in the brainstem and cerebellum) that are interpreted by the brain as movement. Vertigo is one of the most common symptoms in medicine, affecting 30-40% of adults at some point in their lives, and accounting for approximately 5% of all GP consultations. It is classified as peripheral (originating from the inner ear or vestibular nerve — the most common type, representing approximately 80% of cases) or central (originating from the brainstem or cerebellum — rarer but more serious, with red flag features that require urgent investigation). The most important peripheral causes are: benign paroxysmal positional vertigo (BPPV — the single most common cause of vertigo worldwide, accounting for 50% of cases); vestibular neuritis (viral inflammation of the vestibular nerve — causing prolonged acute vertigo without hearing loss); labyrinthitis (viral inflammation of the labyrinth — causing acute vertigo with hearing loss); and Meniere's disease (endolymphatic hydrops — causing episodic vertigo with fluctuating hearing loss, tinnitus, and aural fullness). Central causes include posterior fossa stroke or TIA (posterior circulation), cerebellar haemorrhage, multiple sclerosis, and posterior fossa tumours — these are distinguished from peripheral vertigo by the HINTS examination (Head Impulse test, Nystagmus pattern, Test of Skew). Accurate diagnosis is critical because BPPV is cured by a simple bedside repositioning manoeuvre (Epley), while central vertigo may represent a stroke requiring emergency treatment.

Benign paroxysmal positional vertigo (BPPV): the most common cause of vertigo — caused by displaced calcium carbonate crystals (otoconia or canaliths) from the otolithic membrane of the utricle into one of the semicircular canals (most commonly the posterior semicircular canal — 85% of BPPV cases); otoconia in the canal generate abnormal endolymph currents with head position changes, stimulating cupular deflection and triggering brief vertigo episodes. Triggered by: looking up or to the side, rolling over in bed, bending forward. BPPV affects women twice as often as men; risk increases with age (natural otoconia degeneration), head trauma, prolonged bed rest, and vitamin D deficiency. Vestibular neuritis: acute unilateral inflammation of the vestibular (superior or inferior) division of the vestibulocochlear nerve — presumed viral aetiology (HSV-1 reactivation within the vestibular ganglion — most likely mechanism); causes acute severe continuous vertigo lasting days to weeks; no hearing loss (distinguishes from labyrinthitis); gradual spontaneous central compensation over 4-6 weeks. Labyrinthitis: viral or bacterial inflammation of the labyrinth (inner ear) — causes acute vertigo plus sudden unilateral sensorineural hearing loss; bacterial labyrinthitis is a complication of otitis media or meningitis. Meniere's disease (endolymphatic hydrops): abnormal accumulation of endolymph in the membranous labyrinth — causes recurring episodes of: rotational vertigo (typically lasting 20 minutes to 24 hours); ipsilateral fluctuating low-frequency sensorineural hearing loss; ipsilateral tinnitus (typically roaring or low-pitched); and ipsilateral aural fullness. Episodes are unpredictable and debilitating; over decades, progressive permanent hearing loss develops. Risk factors: autoimmune disease, migraine (migrainous vertigo — the second most common cause of episodic vertigo; associated with other migraine features, no fixed hearing loss), allergic disease, and viral infection. Central causes: posterior circulation stroke or TIA (vertebrobasilar territory — vertebral artery, PICA, AICA, basilar artery) presenting as the 'FIVE D's': diplopia, dysarthria, dysphagia, drop attacks, and dizziness/vertigo; distinguishing features from peripheral vertigo include direction-changing nystagmus, absence of corrective saccade on head impulse test, and skew deviation (vertical misalignment of the eyes); acoustic neuroma (vestibular schwannoma) — slow-growing benign tumour of the vestibular nerve; unilateral sensorineural hearing loss and tinnitus, gradually developing imbalance. Multiple sclerosis (demyelinating plaques in the vestibular pathway — brainstem, cerebellar connections).

Vertigo symptoms are characterised by: the quality of the spinning sensation (rotational vertigo — the world or self spinning — is true vestibular vertigo; swaying, rocking, or tilting suggests either vestibular or non-vestibular origin); duration of vertigo episodes (seconds — BPPV; hours — Meniere's or migrainous vertigo; days — vestibular neuritis; constant — central); triggers (positional change — BPPV; spontaneous with auditory symptoms — Meniere's); and associated symptoms (hearing loss, tinnitus, aural fullness — Meniere's or labyrinthitis; headache — migrainous vertigo or posterior fossa pathology; diplopia, dysarthria, dysphagia — posterior circulation stroke). BPPV: brief episodes of intense rotational vertigo lasting 10-60 seconds, triggered by specific head position changes (looking up, rolling over in bed, bending forward); accompanied by nystagmus (abnormal eye movements); no hearing loss or tinnitus; symptom-free between attacks. Dix-Hallpike test (diagnostic for BPPV): patient rapidly moved from sitting to head-hanging position with head turned 45 degrees to the affected side — triggers rotational nystagmus (torsional, beating toward the lower ear) with latency of 5-15 seconds, fatiguing with repeated testing. Vestibular neuritis: acute onset severe rotational vertigo lasting days; nausea, vomiting; inability to stand without support; no hearing loss; spontaneous nystagmus beating away from the affected ear; positive head impulse test (corrective saccade — vestibulo-ocular reflex deficit). Meniere's disease: episodic rotational vertigo (20 minutes to 24 hours); preceding aural fullness and tinnitus increasing before an attack; post-attack exhaustion lasting hours. HINTS examination (distinguishes peripheral from central acutely): Head Impulse (positive — reassuring, peripheral; negative — concerning for central); Nystagmus (unidirectional, horizontal — peripheral; direction-changing, purely vertical, or torsional in upright — central); Test of Skew (negative — peripheral; positive vertical skew deviation — central).

Clinical diagnosis is the foundation of vertigo assessment. History: the most informative component — duration of individual vertigo attacks; triggers (positional vs. spontaneous); associated auditory symptoms; neurological symptoms; headache pattern; and medication history (many medications cause dizziness and imbalance: aminoglycosides, loop diuretics, antiepileptics, antihypertensives). Dix-Hallpike manoeuvre: the standard diagnostic test for posterior canal BPPV — described above; sensitivity 79-90%, specificity 75%; a positive test (reproducible rotational nystagmus with latency, fatiguing on repeat) confirms posterior canal BPPV and identifies the affected ear. Supine roll test (roll test): for horizontal canal BPPV — patient supine with head in neutral position, then rapidly rolled to each side; reproduces geotropic (towards the floor) or apogeotropic (away from the floor) horizontal nystagmus. Audiometry (pure-tone audiogram): mandatory in vertigo with hearing loss — identifies characteristic low-frequency sensorineural hearing loss of Meniere's disease; high-frequency notch of acoustic neuroma. Tympanometry and acoustic reflexes: assesses middle ear function. Electronystagmography (ENG) / videonystagmography (VNG): records eye movements during caloric testing and positional tests — quantifies vestibular hypofunction; caloric testing (irrigating each ear with warm and cold water) assesses unilateral vestibular function. MRI brain and internal auditory meati (IAM) with gadolinium: indicated for: all cases of unilateral sensorineural hearing loss (exclude acoustic neuroma); suspected central vertigo (history of neurological symptoms, HINTS examination suggesting central cause, headache); progressive or atypical vertigo; and failure of Epley to resolve BPPV (exclude posterior fossa tumour). CT brain (urgent): for acute vertigo with headache and neurological signs — first-line to exclude haemorrhage (MRI posterior fossa is superior for ischaemia). Blood tests: FBC (anaemia), glucose (hypoglycaemia mimics vertigo), thyroid function (hypothyroidism can cause dizziness); anti-cochlear antibodies for autoimmune inner ear disease.

BPPV treatment — canalith repositioning manoeuvres (CRM): the Epley manoeuvre (posterior canal BPPV — the most common type): a series of 5 sequential head position changes through 180 degrees in the plane of the affected posterior canal, each position held for 30-60 seconds to allow gravity to move the displaced otoconia back into the utricle; single Epley session achieves resolution in 80% of posterior BPPV cases at 1 week; repeat if needed — cumulative resolution rate above 90% after 1-3 treatments; no medication required. Semont manoeuvre: alternative for posterior BPPV. Gufoni or Barbecue roll manoeuvre for horizontal canal BPPV. Patients can self-perform the Epley at home after instruction. Vestibular suppressant medications (for acute severe vertigo — not for long-term use): prochlorperazine (Stemetil — 5-10 mg oral or 12.5 mg IM/buccal) — dopamine antagonist; effective antiemetic and vestibular suppressant for acute vertigo and nausea; buccal (Buccastem) useful when unable to swallow due to vomiting; avoid beyond 72 hours as it impairs central vestibular compensation. Cinnarizine, cyclizine, or promethazine — alternative antihistamine vestibular suppressants. Acute vestibular neuritis: short course of oral corticosteroids (prednisolone 100 mg tapering over 3 weeks) may improve long-term vestibular function if started within 3 days of onset; vestibular suppressants for acute symptoms only (maximum 3 days). Vestibular rehabilitation therapy (VRT): graded exercises designed to promote central vestibular compensation by repeatedly exposing the brain to vestibular-visual-proprioceptive mismatches — gaze stability exercises, habituation exercises, and balance training; most effective treatment for chronic vestibular hypofunction after vestibular neuritis; supervised VRT with a physiotherapist achieves faster and more complete compensation than spontaneous recovery alone. Meniere's disease: acute attacks — prochlorperazine for nausea and vertigo; betahistine (16-48 mg three times daily — histamine H3 receptor antagonist; reduces endolymphatic pressure by improving cochlear microvascular blood flow; reduces attack frequency in some patients); low-sodium diet (below 2000 mg/day — reduces endolymph production); diuretics (thiazide or frusemide). Refractory Meniere's: intratympanic gentamicin (chemical labyrinthectomy — ablates vestibular function in the affected ear; highly effective at preventing further attacks but risks permanent unilateral hearing loss); endolymphatic sac decompression surgery (less effective); labyrinthectomy. Migrainous vertigo: treat underlying migraine (topiramate, amitriptyline, propranolol — prophylaxis; triptan for acute attacks). Central vertigo (stroke): emergency thrombolysis or thrombectomy for posterior circulation ischaemic stroke; posterior fossa haematoma — neurosurgical drainage if clinically deteriorating.

Untreated or persistent BPPV: while BPPV is benign, failure to treat leads to chronic positional vertigo that causes significant functional limitation — avoidance of head movements, reduced mobility, fear of falling, and fall-related injuries (fractures, head trauma). Elderly patients with BPPV have a 3-fold increased fall risk and hip fracture rate. Falls and fall-related injuries: vestibular disorders of all types impair postural stability and increase fall risk — particularly significant in elderly patients with osteoporosis; vestibular disorders account for a substantial proportion of the attributable risk for falls and hip fractures in older adults. Chronic vestibular hypofunction: incomplete central compensation after vestibular neuritis causes persistent imbalance, oscillopsia (image instability on head movement), and functional disability in 30-40% of patients; vestibular rehabilitation is essential. Meniere's disease: progressive permanent unilateral sensorineural hearing loss over decades — affecting the full audiometric frequency range in advanced disease; bilateral Meniere's (affects approximately 30-50% of patients) causes bilateral hearing loss and severe imbalance; emotional impact of unpredictable disabling attacks causes anxiety and depression in 40-60% of patients; occupational disability (inability to drive, work at heights, or operate machinery safely). Psychological impact: chronic vertigo from any cause causes significant anxiety, agoraphobia, social withdrawal, depression, and health anxiety — significantly reducing quality of life; cognitive behavioural therapy (CBT) targeted at vestibular symptoms (interoceptive exposure exercises) is highly effective. Misdiagnosed central vertigo: failure to identify posterior circulation stroke or cerebellar haematoma as the cause of vertigo delays emergency treatment and leads to permanent neurological disability or death.

BPPV prevention: vitamin D supplementation may reduce BPPV recurrence — observational studies and a 2020 RCT (Kim et al.) showed that vitamin D supplementation (400-1200 IU daily) significantly reduces BPPV recurrence in patients with deficiency; test serum vitamin D in patients with recurrent BPPV and supplement if below 50 nmol/L. Regular canalith repositioning (self-Epley) practice is effective when patients learn the home technique and repeat it at onset of each recurrent episode. Avoid prolonged bed rest where possible — immobility increases otoconia displacement risk. Meniere's disease management: maintain strict low-sodium diet (below 2000 mg/day) consistently — dietary adherence is the most evidence-supported preventive measure for reducing attack frequency; avoid caffeine, alcohol, and monosodium glutamate (all may trigger attacks); stress management (stress triggers Meniere's attacks in many patients — relaxation techniques, CBT); regular betahistine compliance; maintain adequate hydration. Vestibular rehabilitation: early initiation of graded vestibular exercises after vestibular neuritis or labyrinthitis significantly reduces the duration of disability and prevents chronic vestibular hypofunction — patients should begin gentle gaze stability and habituation exercises as soon as they can tolerate them (within days of acute episode) rather than waiting for spontaneous recovery. Migrainous vertigo prevention: standard migraine prophylaxis (propranolol 40-240 mg/day, amitriptyline 10-75 mg nocte, topiramate 25-100 mg twice daily) significantly reduces migrainous vertigo attack frequency. Avoid vestibulotoxic medications (aminoglycoside antibiotics, loop diuretics at high doses) when alternatives exist; if unavoidable, monitor with serial audiometry and vestibular function tests.

Call 999 or go to A&E immediately for: sudden onset severe vertigo with any of the following neurological features — sudden severe headache (thunderclap), diplopia (double vision), slurred speech, difficulty swallowing, limb weakness or incoordination, facial numbness or droop — these are posterior circulation stroke symptoms and require emergency CT or MRI brain and thrombolysis assessment. Any acute vertigo in a patient with known cardiovascular risk factors (hypertension, diabetes, AF, smoking, previous TIA or stroke) should also be assessed urgently to exclude posterior circulation TIA or stroke. See a GP within 1-2 days for: first episode of acute severe vertigo with vomiting (may be vestibular neuritis or labyrinthitis — early corticosteroid treatment may improve long-term outcomes if started within 3 days); sudden unilateral hearing loss with or without vertigo — sudden sensorineural hearing loss is an otological emergency requiring oral or intratympanic corticosteroids within 72 hours; recurrent episodes of vertigo (each lasting 20 minutes to 24 hours) with hearing loss and tinnitus — possible Meniere's disease requiring investigation. For typical BPPV (brief positional vertigo triggered by lying down, lasting under 60 seconds, no hearing loss, no neurological features): a GP can perform or teach the Epley manoeuvre, or refer to physiotherapy for vestibular rehabilitation. ENT or neurotology referral for: recurrent BPPV not responding to repositioning manoeuvres; suspected Meniere's disease; unilateral hearing loss requiring MRI to exclude acoustic neuroma.